carlsson

Question 1

what are the aims of carlsson’s study?

Answer 1

• provide up to date review of the current status of the dopamine hypothesis
• raise awareness of the potential role of glutamate, serotonin and GABA in SZ
• present suggestions for future drug treatments for a wide range of people with SZ who are ‘treatment resistant’ or experience extreme side effect

Question 2

what is the method used in carlsson’s study?

Answer 2

• article review - researchers looked at secondary data from 33 studies, 14 conducted by Carlsson.
• methods used included animal studies (rats)/ PET & SPECT scans to measure neurotransmitter activity and drug trials.

Question 3

carlsson - dopamine hypothesis revisited

Answer 3

• there is continuing evidence to support this, PET scans show amphetamines (stimulant drug-speed) is a dopamine agonist which increases dopa activity and enhanced SZ symptoms in people with SZ more than compared to age-matched controls.
• however doesn’t apply to all people with sz

Question 4

carlsson - beyond dopamine

Answer 4

• some ppl with SZ have ‘normal’ dopamine activity
• this suggests high dopa can explain symptoms in a subgroup of patients, but not all, other subgroups have dysfunction in different neurotransmitters, not just dopa
• participants in this research were in ‘acute’ episodes and not ‘chronic’

Question 5

carlsson - glutamate hypothesis

Answer 5

• hypoglutaminergic activity may cause SZ

research in rats found PCP ‘angel dust’ causes SZ-liek symptoms because…
* it is a powerful antagonist of glutamate receptors (NMDA receptors), so it blocks them, causing low levels of glutamate, causing high levels of dopamine

• suggests excess dopa is a byproduct of dysfunction of glutamate

Question 6

carlsson - gluta, sero and dopa

Answer 6

dopa levels may be controlled by serotonin and glutamate
* high sero = high dopa

low levels of glutamate cause high levels of serotonin which causes high levels of dopamine
* low gluta = high sero = high dopa

MESOLIMBIC PATHWAY
Glutamate acts as a break between it signals to GABA to inhibit dopamine production

IF THIS PROCESS ISN’T WORKING PROPERLY

and the levels of glutamate are too low, this causes low levels of GABA which causes excess levels of dopamine which causes POSITIVE symptoms
low gluta=low gaba=high dopa

MESOCORTICAL PATHWAY
Glutamate acts as an accelerator
IF THIS PROCESS ISN’T WORKING PROPERLY
and glutmate levels fall too low this causes low levels of dopa which causes NEGATIVE symptoms

Question 7

carlsson - future treatment

Answer 7

• different symptoms sets could be the result of differing neurotransmitter dysfunction
• people with different symptom sets couild be treated with a combination of drugs targetting different neurotransmitters
• Clozapine is an example of this - it blocks dopamine (binds loosely to D2 receptors) as well as serotonin receptors, alleviating + and - symptoms and is used for treatment-resistant cases
• more dopamine agonists need to be developed which avoid the negative side-effects of current antipsychotics

Question 8

carlsson - conclusions

Answer 8

• A number of subpopulations exist among SZ patients
• More attention should be focussed on other neurotransmitters (eg. acetylcholine and GABA) and other pathways in the brain to identify a more sufficient explanation of SZ

Question 9

carlsson - reliability

Answer 9

P - High Reliability

E - PET/SPECT scans show dopa agonists (amphetamines) enhance SZ-like symptoms in ppl with SZ more than compared to age-matched controls.

T - Therefore it is replicable because it makes use of a standardised and objective measurement, can be checked for consitent results

Question 10

carlsson - internal validity

Answer 10

P: Internal validity

E: Achieved using control groups. Amphetamine enhances SZ-like symptoms in ppl with SZ more than compared to age-matched control

T: Valid because accurate cause and effect conclusions about excess dopamine can made from this comparison

Question 11

carlsson - application

Answer 11

P: Application to real life

E: Conclusions will lead to development of more effective drugs with fewer side effects tailored to subpopulations of SZ by targeting multiple neuro.

T: Improve the quality of life of individuals who were resistant to traditional drugs

Question 12

carlsson - high scientific status

Answer 12

P: High scientific status:

E: Revisited original dopa hypo, suggested need to move ‘beyond’ dopa, focus on gluta based on empirical evidence, future research will create new hypo

T: Hypothetico Deductive model (write hypo, test hypo, improve hypo)
Credible research

Question 13

carlsson - generalisability

Answer 13

P: Low Generalisability

E: studies reviewed measured pps with acute sz (severe & sudden onset) but not chronic SZ

T: Explanations and medication based on this research may not be representative of wider SZ population

Question 14

carlsson - generalisability to humans limited by animals

Answer 14

P: Generalisability to humans limited by use of animals

E: Rats and mice given NDMA antagonist (blocks gluta), SZ-like symptoms measured

T: Application to humans limited because neuro. activity in brains of rats similar but not exactly the same

Question 15

carlsson - second hand data

Answer 15

P: Second hand data

E: 19 pieces of second hand data Carlsson cannot be sure of the extent to which data was collected and analysed objectively because he didn’t collect it himself

T: May be issues with reliability and validity

Question 16

carlsson - reductionist

Answer 16

P: Biologically reductionist:

E: Findings + conc ignore role of genes and social causation factors (social adversity/urbanicity) because it reduces SZ down to neuro, so doesn’t consider how environment interacts with neuro

T: Fails to be holistic and consider how multiple factors interact, lowers validity of our knowledge of SZ